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Blood, 1 April 2007, Vol. 109, No. 7, pp. 2961-2967. Prepublished online as a Blood First Edition Paper on November 21, 2006; DOI 10.1182/blood-2006-08-041772. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2006-08-041772v1 109/7/2961    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Sakurai, D. Articles by Kobata, T. Search for Related Content PubMed PubMed Citation Articles by Sakurai, D. Articles by Kobata, T. Related Collections Immunobiology Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY TACI regulates IgA production by APRIL in collaboration with HSPG Daisuke Sakurai1, Hidenori Hase1, Yumiko Kanno1, Hidefumi Kojima1, Ko Okumura2, and Tetsuji Kobata1,3 1 Department of Immunology and 3 Research Institute for Neuroimmunological Diseases, Dokkyo Medical University School of Medicine, Tochigi, Japan; 2 Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan Transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) is a member of the tumor necrosis factor (TNF) receptor family that serves as a receptor for B-cell activating factor of the TNF family (BAFF) and as a proliferation-inducing ligand (APRIL). Although TACI is reported to function as a positive or negative regulator for B-cell responses, its roles remain elusive. Experiments using TACI siRNA into B cells indicated that TACI positively regulated APRIL-induced IgA production in collaboration with heparan sulfate proteoglycans (HSPG). Furthermore, TACI negatively regulated BAFF-induced B-cell proliferation and production of IgA and IgG. In addition, B cells treated with heparitinase to denature HSPG showed that HSPG is essential for APRIL-induced B-cell responses such as B-cell proliferation, IgG and IgA production, induction of activation-induced cytidine deaminase (AID), and noncanonical NF-B2. In contrast, phosphorylation of physiological AID kinase, protein kinase A (PKA), was dependent on TACI. Importantly, coligation of TACI and HSPG by specific antibodies, but not by TACI or HSPG ligation itself, could induce the phosphorylation of PKA and IgA production instead of APRIL. Our findings indicate that simultaneous binding of TACI and HSPG on B cells with APRIL is crucial for IgA production. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Gupta, S. R. Dillon, S. C. Ziesmer, A. L. Feldman, T. E. Witzig, S. M. Ansell, J. R. Cerhan, and A. J. Novak A proliferation-inducing ligand mediates follicular lymphoma B-cell proliferation and cyclin D1 expression through phosphatidylinositol 3-kinase-regulated mammalian target of rapamycin activation Blood, May 21, 2009; 113(21): 5206 - 5216. [Abstract] [Full Text] [PDF] F. C. Kimberley, L. van Bostelen, K. Cameron, G. Hardenberg, J. A. Marquart, M. Hahne, and J. P. Medema The proteoglycan (heparan sulfate proteoglycan) binding domain of APRIL serves as a platform for ligand multimerization and cross-linking FASEB J, May 1, 2009; 23(5): 1584 - 1595. [Abstract] [Full Text] [PDF] C. Bossen, T. G. Cachero, A. Tardivel, K. Ingold, L. Willen, M. Dobles, M. L. Scott, A. Maquelin, E. Belnoue, C.-A. Siegrist, et al. TACI, unlike BAFF-R, is solely activated by oligomeric BAFF and APRIL to support survival of activated B cells and plasmablasts Blood, February 1, 2008; 111(3): 1004 - 1012. [Abstract] [Full Text] [PDF]

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